Evidence map›Paper›PMID 22988095›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

O-GlcNAc cycling mutants modulate proteotoxicity in Caenorhabditis elegans models of human neurodegenerative diseases.

Peng Wang, Brooke D Lazarus, Michele E Forsythe, Dona C Love, Michael W Krause, John A Hanover

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 2 pooled it
3.6field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

63 citing papers in PubMed, 2 syntheses or guidelines pooled it, 95 citations in OpenAlex.

  1. Guideline
  2. Guideline
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Unraveling Molecular Targets for Neurodegenerative Diseases ThroughInternational journal of molecular sciences · 2025
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. ProteinMetabolites · 2022
    Review
  17. Thermal Proteome Profiling Reveals the O-GlcNAc-Dependent Meltome.Journal of the American Chemical Society · 2022
    Article
  18. Review
  19. Pathophysiological interplay betweenProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  20. Review

3 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Peng WangLaboratories of Cell and Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Brooke D Lazarus
Michele E Forsythe
Dona C Love
Michael W Krause
John A Hanover
National Institute of Diabetes and Digestive and Kidney Diseases · US

Funding

Targeted disruption the enzymes of O-GlcNAc cycling: Animal models of DiseaseZIADK060101 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI HANOVER, JOHN A. · 2009 to 2025
$25.7M
Nutrient Flux and DevelopmentZIADK036133 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI KRAUSE, MICHAEL · 2009 to 2020
$9.1M
Intramural NIH HHS
6 · The paper itself

Abstract

O-GlcNAcylation is an abundant posttranslational modification in the brain implicated in human neurodegenerative diseases. We have exploited viable null alleles of the enzymes of O-GlcNAc cycling to examine the role of O-GlcNAcylation in well-characterized Caenorhabditis elegans models of neurodegenerative proteotoxicity. O-GlcNAc cycling dramatically modulated the severity of the phenotype in transgenic models of tauopathy, amyloid β-peptide, and polyglutamine expansion. Intriguingly, loss of function of O-GlcNAc transferase alleviated, whereas loss of O-GlcNAcase enhanced, the phenotype of multiple neurodegenerative disease models. The O-GlcNAc cycling mutants act in part by altering DAF-16-dependent transcription and modulating the protein degradation machinery. These findings suggest that O-GlcNAc levels may directly influence neurodegenerative disease progression, thus making the enzymes of O-GlcNAc cycling attractive targets for neurodegenerative disease therapies.

Indexed as

Disease Models, AnimalMutationAcetylglucosamineAllelesAnimalsCaenorhabditis elegansHumansNeurodegenerative DiseasesProteolysisAcetylglucosamine

Identifiers

PMID22988095
PMCPMC3491483
OpenAlexW1988250463

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.